Mutation rates are under genetic control. In bacteria and yeast, the frequency of induced mutations can be either increased or decreased by blocking one or another pathway of DNA repair. This project is designed to determine the relationship between DNA repair and mutagenesis in Drosophila melanogaster. Three approaches are being taken: (1) A mutant which increases the mutation frequency (a mutator) has been identified, mapped, and characterized. This mutator blocks repair of chromosome breaks specifically in oocytes, thereby allowing a previously undescribed repair process to be observed. In this process broken chromosomes are "healed", allowing the recovery of terminal deletions. (2) The interaction of DNA repair-defective mutants and transposable elements has been observed in double mutant combinations. None of the repair-defective mutants examined to date influence the rates of transposon-induced mutation or recombination, although mutants at the mei-41 locus prevent the transmission of transposon-bearing chromosomes. (3) Aneuploidy is being examined as a genetic endpoint. Chemicals that induce aneuploidy are being identified as probes to investigate mitosis and meiosis.